Abstract

Abstract Lung cancer is the most common cause of cancer related death in men and second most common in women, after breast cancer. It is known to be responsible for 1.3 million deaths worldwide annually. The p53 gene, is a tumor suppressor gene, i.e. its activity stops the formation of tumors. The gene has been mapped to chromosome 17. In the cell, p53 protein binds DNA, which in turn stimulates another gene to produce a protein called p21 that interacts with a cell division-stimulating protein (cdk2). When p21 is complexed with cdk2 the cell cannot pass through to the next stage of cell division. In present study we check Association of P53 polymorphism with lung cancer in Pakistani population. Polymorphisms in human P53 gene (16bp duplication in intron 3) were studied in patients with lung cancer and controls. Three types of genotypes were seen, homozygous insertion (1\1), homozygous deletion (2\2) and heterozygous insertion/deletion (1/2). Frequency of 1/2 allele was 0.2 in controls and 0.32 in lung cancer patients. This difference is statistically significant (P = 0.053, 95 CI). Our study further showed that smoking increases the risk of lung cancer. Study of polymorphism in p53 gene will help in understanding the patho-physiology of the lung cancer and will open new fronts in future therapeutics. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2011 Nov 12-16; San Francisco, CA. Philadelphia (PA): AACR; Mol Cancer Ther 2011;10(11 Suppl):Abstract nr B91.

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